Evidence map›Paper›PMID 35112129›Full record

ArticleDevelopment (Cambridge, England)2022

An essential function for autocrine hedgehog signaling in epithelial proliferation and differentiation in the trachea.

Wenguang Yin, Andreas Liontos, Janine Koepke, Maroua Ghoul, Luciana Mazzocchi, Xinyuan Liu, Chunyan Lu, Haoyu Wu, Athanasios Fysikopoulos, Alexandros Sountoulidis and 5 more

Open access · hybridAbstract read
In one paragraph

Article in Development (Cambridge, England), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.2field-weighted citation impact, top 22% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

14 citing papers in PubMed, 14 citations in OpenAlex.

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  12. The lung mesenchyme in development, regeneration, and fibrosis.The Journal of clinical investigation · 2023
    Review
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  14. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

15 authors at 8 institutions in 3 countries.

Wenguang YinCardio-Pulmonary Institute, Member of the German Center for Lung Research (DZL), University of Giessen and Marburg Lung Center (UGMLC), Justus Liebig University of Giessen, Giessen 35392, Germany.
Andreas LiontosDepartment of Molecular Biosciences, The Wenner-Gren Institute, Stockholm University, S-10691 Stockholm, Sweden.
Janine KoepkeCardio-Pulmonary Institute, Member of the German Center for Lung Research (DZL), University of Giessen and Marburg Lung Center (UGMLC), Justus Liebig University of Giessen, Giessen 35392, Germany.
Maroua GhoulCardio-Pulmonary Institute, Member of the German Center for Lung Research (DZL), University of Giessen and Marburg Lung Center (UGMLC), Justus Liebig University of Giessen, Giessen 35392, Germany.
Luciana MazzocchiCardio-Pulmonary Institute, Member of the German Center for Lung Research (DZL), University of Giessen and Marburg Lung Center (UGMLC), Justus Liebig University of Giessen, Giessen 35392, Germany.
Xinyuan LiuState Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Disease, Guangzhou Institute of Respiratory Health, the First Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong 510182, People's Republic of China.
Chunyan LuState Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Disease, Guangzhou Institute of Respiratory Health, the First Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong 510182, People's Republic of China.
Haoyu WuState Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Disease, Guangzhou Institute of Respiratory Health, the First Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong 510182, People's Republic of China.
Athanasios FysikopoulosCardio-Pulmonary Institute, Member of the German Center for Lung Research (DZL), University of Giessen and Marburg Lung Center (UGMLC), Justus Liebig University of Giessen, Giessen 35392, Germany.
Alexandros SountoulidisDepartment of Molecular Biosciences, The Wenner-Gren Institute, Stockholm University, S-10691 Stockholm, Sweden.
Werner SeegerCardio-Pulmonary Institute, Member of the German Center for Lung Research (DZL), University of Giessen and Marburg Lung Center (UGMLC), Justus Liebig University of Giessen, Giessen 35392, Germany.
Clemens RuppertCardio-Pulmonary Institute, Member of the German Center for Lung Research (DZL), University of Giessen and Marburg Lung Center (UGMLC), Justus Liebig University of Giessen, Giessen 35392, Germany.
Andreas GüntherCardio-Pulmonary Institute, Member of the German Center for Lung Research (DZL), University of Giessen and Marburg Lung Center (UGMLC), Justus Liebig University of Giessen, Giessen 35392, Germany.
Didier Y R StainierDepartment of Developmental Genetics, Max Planck Institute for Heart and Lung Research, Member of the German Center for Lung Research (DZL), Bad Nauheim 61231, Germany.
Christos SamakovlisCardio-Pulmonary Institute, Member of the German Center for Lung Research (DZL), University of Giessen and Marburg Lung Center (UGMLC), Justus Liebig University of Giessen, Giessen 35392, Germany.
Justus-Liebig-Universität Gießen · DEUniversities of Giessen and Marburg Lung Center · DEGerman Center for Lung Research · DEGuangzhou Medical University · CNScience for Life Laboratory · SECardio-Pulmonary Institute · DEState Key Laboratory of Respiratory Disease · CNStockholm University · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The tracheal epithelium is a primary target for pulmonary diseases as it provides a conduit for air flow between the environment and the lung lobes. The cellular and molecular mechanisms underlying airway epithelial cell proliferation and differentiation remain poorly understood. Hedgehog (HH) signaling orchestrates communication between epithelial and mesenchymal cells in the lung, where it modulates stromal cell proliferation, differentiation and signaling back to the epithelium. Here, we reveal a previously unreported autocrine function of HH signaling in airway epithelial cells. Epithelial cell depletion of the ligand sonic hedgehog (SHH) or its effector smoothened (SMO) causes defects in both epithelial cell proliferation and differentiation. In cultured primary human airway epithelial cells, HH signaling inhibition also hampers cell proliferation and differentiation. Epithelial HH function is mediated, at least in part, through transcriptional activation, as HH signaling inhibition leads to downregulation of cell type-specific transcription factor genes in both the mouse trachea and human airway epithelial cells. These results provide new insights into the role of HH signaling in epithelial cell proliferation and differentiation during airway development.

Indexed as

Cell DifferentiationCell ProliferationAnimalsAutocrine CommunicationCells, CulturedDown-RegulationEmbryo, MammalianEpithelial CellsHedgehog ProteinsHumansLungMiceMice, KnockoutSignal TransductionSmoothened ReceptorTracheaHedgehog ProteinsSmoothened ReceptorSmo protein, mouseTranscription FactorsAirway epithelial cellsSmoothenedSonic hedgehogTracheaTracheomalacia

Identifiers

PMID35112129
PMCPMC8918789
OpenAlexW4225762472

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.